{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,14]],"date-time":"2026-08-14T11:35:09Z","timestamp":1786707309766,"version":"build-2736575974"},"reference-count":55,"publisher":"Akademiai Kiado Zrt.","issue":"2","license":[{"start":{"date-parts":[[2026,8,14]],"date-time":"2026-08-14T00:00:00Z","timestamp":1786665600000},"content-version":"unspecified","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["www.akjournals.com"],"crossmark-restriction":true},"short-container-title":["ATR"],"published-print":{"date-parts":[[2026,8,14]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background and Aim<\/jats:title>\n                    <jats:p>\n                      Aging in mammals is a complex, multifaceted process involving the progressive decline of physiological functions, in which energy metabolism plays a pivotal role.\n                      <jats:italic>\u03b2<\/jats:italic>\n                      -oxidation\u2014the primary pathway for converting fatty acids into energy\u2014is tightly linked to aging and to female reproductive senescence. In the present study, we investigated how ovarian tissue remodels hepatic proteins central to the\n                      <jats:italic>\u03b2<\/jats:italic>\n                      -oxidation pathway.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      Liver proteomes were analyzed in CBA\/J control mice at 4,\u00a013, 23, and 27 months of age and compared with those of 23-month-old mice that received transplants of young ovarian tissue at 13 months.\n                      <jats:italic>\u03b2<\/jats:italic>\n                      -oxidation proteins were quantified using high-resolution mass spectrometry. Serum triglycerides were measured enzymatically, and metabolic cage analyses were performed\u00a0to assess substrate utilization and energy balance.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Ovarian tissue transplantation substantially modulates the expression of\n                      <jats:italic>\u03b2<\/jats:italic>\n                      -oxidation-related proteins and reduces systemic lipid accumulation in aged mice. These proteomic shifts are consistent with enhanced metabolic efficiency and decreased oxidative stress\u2014mechanisms well-established as drivers of extended health span and longevity. Results apply to menopause dyslipidemia, insulin resistance, metabolic syndrome, NAFLD, and aging. Transplants reduce\n                      <jats:italic>\u03b2<\/jats:italic>\n                      -oxidation proteins and triglycerides, improving hepatic lipid clearance and steatosis risk. Identifying ovarian signals enables non-surgical mimics via peptides or modulators. Changes align with PPAR\u03b1 agonists, CPT1 modulators, mitochondria-targeted antioxidants (MitoQ), and NAD\n                      <jats:sup>+<\/jats:sup>\n                      \/sirtuin pathways\u2014offering testable routes to replicate ovarian benefits.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>\n                      Ovarian-derived signals induce metabolic reprogramming in aged mice, characterized by reduced\n                      <jats:italic>\u03b2<\/jats:italic>\n                      -oxidation protein expression, decreased triglyceride accumulation, and improved metabolic efficiency. These findings provide a molecular framework for understanding how ovarian-derived factors may govern metabolism and organismal health during aging, with potential implications for interventions targeting age-related metabolic decline.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1556\/1661.2026.00112","type":"journal-article","created":{"date-parts":[[2026,5,8]],"date-time":"2026-05-08T14:00:49Z","timestamp":1778248849000},"page":"106-117","update-policy":"https:\/\/doi.org\/10.1556\/policypage.crossmark.crossref.2","source":"Crossref","is-referenced-by-count":0,"title":["Ovarian-derived signals reprogram hepatic lipid\u00a0metabolism in aging: Implications for therapeutic targeting of metabolic dysfunction"],"prefix":"10.1556","volume":"1","author":[{"ORCID":"https:\/\/orcid.org\/0009-0000-5777-7871","authenticated-orcid":true,"given":"Nathan D.","family":"McCoy","sequence":"first","affiliation":[{"name":"College of Veterinary Medicine, Department of Veterinary Clinical and Life Sciences, Center for Integrated BioSystems, Utah State University, Logan, UT, 84322, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7409-8918","authenticated-orcid":true,"given":"Michael T.","family":"Kinter","sequence":"additional","affiliation":[{"name":"Aging and Metabolism Research Program, Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3410-2860","authenticated-orcid":true,"given":"Augusto","family":"Schneider","sequence":"additional","affiliation":[{"name":"Faculdade de Nutri\u00e7\u00e3o, Universidade Federal de Pelotas, Pelotas-RS, Brasil"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4145-9304","authenticated-orcid":true,"given":"Fabiola","family":"Santos","sequence":"additional","affiliation":[{"name":"Faculdade de Nutri\u00e7\u00e3o, Universidade Federal de Pelotas, Pelotas-RS, Brasil"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-8483-930X","authenticated-orcid":true,"given":"Michal M.","family":"Masternak","sequence":"additional","affiliation":[{"name":"College of Medicine, Burnett School of Biomedical Sciences, University of Central Florida, Orlando, FL, USA"},{"name":"Department of Head and Neck Surgery, Poznan University of Medical Sciences, Poznan, Poland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2459-1186","authenticated-orcid":true,"given":"Jeffrey B.","family":"Mason","sequence":"additional","affiliation":[{"name":"College of Veterinary Medicine, Department of Veterinary Clinical and Life Sciences, Center for Integrated BioSystems, Utah State University, Logan, UT, 84322, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"425","reference":[{"key":"B1","series-title":"Annu Rev Physiol","doi-asserted-by":"publisher","first-page":"23","DOI":"10.1146\/annurev-physiol-021115-105045","article-title":"The biochemistry and physiology of mitochondrial fatty acid \u03b2-oxidation and its genetic disorders","volume":"78","author":"Houten SM","year":"2016","unstructured":"Houten SM, Violante S, Ventura FV, Wanders RJA. 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